News Release

News tips from the Journal of Neuroscience

Peer-Reviewed Publication

Society for Neuroscience

  1. BMP Signaling and Synaptic Plasticity
    Mu Sun, Mark J. Thomas, Rachel Herder, M. Lisa Bofenkamp, Scott B. Selleck, and Michael B. O’Connor

    Bone morphogenic protein (BMP) has diverse functions in cell signaling from development to cell death. This week, Sun et al. focused on its possible role in synaptic plasticity by targeting the endogenous BMP antagonist chordin. The BMPRII receptor protein was expressed throughout the hippocampus in wild-type mice, as was chordin. Brain slices from mice lacking Chordin (Chrd-/-) had enhanced paired-pulse facilitation and an increased frequency of miniature EPSCs, consistent with a presynaptic site of action for BMP. Nerve terminals in Chrd-/- mice also had an increase in docked vesicles. Perfusion of BMP2 in wild-type slices mimicked the effects seen in slices from Chrd-/- mice. The effects on plasticity and behavior were complex. Long-term potentiation was enhanced in Chrd-/- slices with high-frequency stimulation, but not with theta burst or pairing protocols; and mutant mice showed improved learning in the water maze, but impairment in the Y maze.

  2. Reducing Oligodendrocyte Apoptosis after Spinal Cord Injury
    Tae Y. Yune, Jee Y. Lee, Gil Y. Jung, Sun J. Kim, Mei H. Jiang, Young C. Kim, Young J. Oh, George J. Markelonis, and Tae H. Oh

    Traumatic spinal cord injury (SCI) leads not only to neuronal loss, but also to apoptosis of oligodendrocytes and subsequent demyelination. This week, Yuneet al. tried to connect the dots between neuroprotection afforded by the antibiotic minocycline, inhibition of microglia activation, and apoptotic signaling through the p75 neurotrophin receptor (p75NTR). Five days after a contusion injury at T10/11 in adult rats, the spinal cord showed elevated levels of proNGF (nerve growth factor). Phosphorylated p38 protein-activated mitogen kinase (p-p38MAPK), an indicator of microglia activation, also increased after SCI. In vitro, the activated microglia produced pro-nerve growth factor (proNGF), which binds to the p75NTR receptor and triggers apoptosis in oligodendrocytes. By several measures, minocycline treatment was effective. It reduced p-p38MAPK and proNGF in microglia as well as p75NTR expression in oligodendrocytes; it reduced axonal and myelin loss after injury; and treated rats had better recovery of hindlimb locomotor function.

  3. News for the Left-Handed
    Stefan Klöppel, Anna Vongerichten, Thilo van Eimeren, Richard S. J. Frackowiak, and Hartwig R. Siebner

    Most of us (90%) do just about every complex manual task with our right hand. Being left-handed in a right-handed world has its advantages and disadvantages. One seeming disadvantage is that some lefties are forced as children to become right-handed. In this week’s Journal, Klöppel et al. investigated the changes that occur as a consequence of retraining, not only for handwriting but also for more general manual tasks. Using fMRI (functional magnetic resonance imaging), the authors compared brain activity between right-handers, left-handers, and converted left-handers. Converted left-handers performing a simple button press displayed increased activity in the SM1 (primary sensorimotor hand area) and the caudal PMd (dorsal premotor cortex) of the nondominant left hemisphere. Thus, the switch in handedness resulted in a reorganization of the executive motor system controlling even simple hand movements. However, higher-order sensorimotor areas were not affected by retraining. So is it better to fight than switch"

  4. The Benefits of Sleep in a Mouse Model of HD
    Patrick N. Pallier, Elizabeth S. Maywood, Zhiguang Zheng, Johanna E. Chesham, Alexei N. Inyushkin, Richard Dyball, Michael H. Hastings, and A. Jennifer Morton

    We usually think of Huntington’s disease (HD) as involving abnormal movements (chorea) and cognitive impairments. However, these patients also show disrupted circadian rhythms. Thus, Pallier et al. compared HD model R6/2 mice with wild-type mice to see how disrupted circadian rhythms might affect cognitive performance. As expected, activity–rest cycles in R6/2 mice became irregular with age, as did expression of the circadian proteins mPER1 and mPER2 in the suprachiasmatic nucleus (SCN). In slices, however, the electrophysiological and molecular clockwork of the SCN appeared intact in R6/2 mice, suggesting that the intrinsic SCN circuitry was functioning normally. Hypnotic doses of sedative drug normalized the sleep–wake cycle and improved cognitive performance on the two-choice swim test in the R6/2 mice and regulated their expression of SCN circadian genes. Although not a cure for HD, symptomatic treatment for disrupted sleep would appear to have its benefits.

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